Effect of two intensive statin regimens on progression of coronary disease.

By Stephen J. Nicholls, Christie M. Ballantyne, P. Barter, M. John Chapman, Raimund M. Erbel, Peter Libby, J. Raichlen, K. Uno, Marilyn Borgman, K. Wolski and 1 more. New England Journal of Medicine, 2011

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BACKGROUND Statins reduce adverse cardiovascular outcomes and slow the progression of coronary atherosclerosis in proportion to their ability to reduce low-density lipoprotein (LDL) cholesterol. However, few studies have either assessed the ability of intensive statin treatments to achieve disease regression or compared alternative approaches to maximal statin administration. METHODS We performed serial intravascular ultrasonography in 1039 patients with coronary disease, at baseline and after 104 weeks of treatment with either atorvastatin, 80 mg daily, or rosuvastatin, 40 mg daily, to compare the effect of these two intensive statin regimens on the progression of coronary atherosclerosis, as well as to assess their safety and side-effect profiles. RESULTS After 104 weeks of therapy, the rosuvastatin group had lower levels of LDL cholesterol than the atorvastatin group (62.6 vs. 70.2 mg per deciliter [1.62 vs. 1.82 mmol per liter], P<0.001), and higher levels of high-density lipoprotein (HDL) cholesterol (50.4 vs. 48.6 mg per deciliter [1.30 vs. 1.26 mmol per liter], P=0.01). The primary efficacy end point, percent atheroma volume (PAV), decreased by 0.99% (95% confidence interval [CI], -1.19 to -0.63) with atorvastatin and by 1.22% (95% CI, -1.52 to -0.90) with rosuvastatin (P=0.17). The effect on the secondary efficacy end point, normalized total atheroma volume (TAV), was more favorable with rosuvastatin than with atorvastatin: -6.39 mm(3) (95% CI, -7.52 to -5.12), as compared with -4.42 mm(3) (95% CI, -5.98 to -3.26) (P=0.01). Both agents induced regression in the majority of patients: 63.2% with atorvastatin and 68.5% with rosuvastatin for PAV (P=0.07) and 64.7% and 71.3%, respectively, for TAV (P=0.02). Both agents had acceptable side-effect profiles, with a low incidence of laboratory abnormalities and cardiovascular events. CONCLUSIONS Maximal doses of rosuvastatin and atorvastatin resulted in significant regression of coronary atherosclerosis. Despite the lower level of LDL cholesterol and the higher level of HDL cholesterol achieved with rosuvastatin, a similar degree of regression of PAV was observed in the two treatment groups. (Funded by AstraZeneca Pharmaceuticals; ClinicalTrials.gov number, NCT000620542.).

Subfields: Cancer Research, Surgery

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In Cancer Research

1. Jan Boren
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3. I. Graham
4. Klaus Ley
5. D. Wolf
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1. Erling Falk
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Citations in the corpus

• Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel (2017, background): “8 mmol/L (70 mg/dL) (Figure 5B).(35,36) Importantly, other therapies that reduce LDL-C without inhibiting HMG-CoA reductase have also been shown to reduce the risk of cardiovascular events in large randomized cardiovascular outcome trials.”
• Mechanisms of plaque formation and rupture. (2014, background): “Plaque Vulnerability To predict which plaques are at risk of precipitating thrombosis and to understand the mechanisms leading to their formation, much effort has been put into recognizing the pathological features of vulnerable plaques (or synonymously thrombosis-prone or high-risk plaques): those ”
• Immunity and Inflammation in atherosclerosis (2019, background): “Statins can prevent, reduce, and even reverse atherosclerotic plaque burden.(178) Monoclonal antibodies to PCSK9 lower LDL cholesterol even more dramatically by blocking LDL degradation(179,180) without apparent impact on levels of CRP levels,(181) a biomarker of systemic inflammation.”